Pharm MS Flashcards
Describe the formation/pathway and function of: LTC,D,E4: LTB4 PGI2: PGE1: PGE2: PGF2: TXA2:
Phospholipase A2 converts membrane phospholipids into Arachidonic acid.
Lipoxygenase converts AA into 5-HPETE then into LTC,D,E4 and LTB4
COX-1,2 convert AA into prostacyclin, prostaglandins, and thromboxane.
LTC,D,E4: Incr. bronchial tone
LTB4: Incr. neutrophil chemotaxis
PGI2: Decr. platelet aggregation, decr. vasc. tone
PGE1: Decr. vascular tone
PGE2: incr. uterine tone
PGF2: incr. uterine tone
TXA2: Incr. platelet aggregation, incr. vascular tone
What is the mechanism of acetaminophen? Where is it inactivated? Clinical use? Toxicity? Antidote?
Reversibly inhibits COX, mostly in CNS
Inactivated peripherally
Antipyretic, analgesic
Not antiinflammatory
Used instead of aspirin to avoid Reye syndrome
Overdose leads to hepatic necrosis; NAPQI depletes glutathione and forms toxic tissue byproducts in liver
N-acetylcysteine: regenerates glutathione
What ist he mechanism of aspirin? Clinical use/doses? Toxicity? Chronic toxicity? Overdose?
Irreversibly inhibits COX via acetylation
Decr. synth of TXA2 and PGs
Incr. bleeding time
No effect on PT/PTT
Low dose=decr. platelet aggregation
Intermediate=antipyretic, analgesic
High=antiinflammatory
Gastric ulceration, tinnitus
Acute renal failure, interstitial nephritis
Reye syndrome
Resp alk early, the to mixed.
What is the mechanism of celecoxib? How does it differ from NSAIDs in affects? Clinical use? toxicity?
Reversibly inhibits COX 2, found in inflammatory cells and vasc endothelium and mediates inflammation and pain; spares COX-1 which helps maintain the gastric mucosa.
No corrosive effects on GI lining and spares platelet function.
RA, osteoarthritis
Incr. risk of thrombosis, sulfa allergy
What type of drugs are ibuprofen, naproxen, indomethacin (1), ketorolac, diclofenac? mechanism? Clinical use ? Of 1? Toxicity?
NSAIDS
Reversibly inhibit COX. Block PG synth
Antipyretic, analgesic, antiinflammatory
1=used to close PDA
Interstitial nephritis, gastric ulcer, renal ischemia (PGs vasodilate afferent arteriole)
What type of drug is alendronate? Mechanism? Clinical use? Toxicity?
Bisphosphonate
Pyrophosphate analog; bind hydroxyapatite in bone, inhibiting osteoclast activity
Osteoporosis, Hypercalcermia, Paget disease of bone
Corrosive esophagitis (take with water, remain upright for 30 min) Osteonecrosis of jaw
What is the mechanism of teriparatide? clincal use? Toxicity?
Recombinant PTH analog given subQ daily.
Incr. osteoblast activity
Osteoporosis
Incr. bone growth compared to antiresorptive therapies
Transient hypercalcemia. May increase risk of osteosarcoma
What are the chronic gout drugs? Acute gout drugs? What should be avoided in acute gout?
Allopurinol
Febuxostat
Pegloticase
Probenecid
NSAIDS
Glucocorticoids
Colchicine
Salicylates
What is the mechanism of allopurinol? Clinical uses? Drug interactions?
Inhibits XO after being converted to alloxanthine
Decr. conversion of xanthine to uric acid
Chronic gout
Lymphoma and leukemia to avoid lysis associated urate nephropathy
Incr. conc. of azathioprine and 6MP (metabolized by XO)
What is the mechanism of febuxostat? Clinical use?
Inhibits XO
Chronic gout
What is the mechanism of pegloticase? Use?
Recombinant uricase that catalyzes metabolism of uric acid to allantoin (more water soluble)
Chronic gout
What is the mech of probenecid? Use? sx?
Inhibits absorption of uric acid in PCT (also secretion of penicillin)
Can precipitate uric acid calculi
What are the NSAIDS used for acute gout?
Naproxen, indomethacin
What is admin of glucocorticoids like in acute gout?
oral or intra articular
What is the mechanism of colchicine? Sx? Uses?
Binds and stabilizes tubulin to inhibit microtubule polymerization, impairing neutrophil chemotaxis and degranulation.
Acute and prophylactic value
